Can thromboelastography (TEG) identify specific clotting factor deficiencies or provide quantitative values for individual clotting factors?

TEG Cannot Identify Specific Clotting Factor Deficiencies

Thromboelastography (TEG) provides a global assessment of hemostasis but cannot identify specific clotting factor deficiencies or provide quantitative values for individual clotting factors. 1 This is a critical limitation that clinicians must understand to avoid mismanagement based on TEG results alone.

What TEG Actually Measures

TEG assesses the viscoelastic properties of whole blood clot formation through several parameters 1:

• R time (Reaction time): Measures time to initial fibrin formation, reflecting clot initiation 2
• K time (Kinetics): Time from clot initiation to reach 20mm clot width 2
• Alpha angle: Rate of clot formation 2
• Maximum Amplitude (MA): Maximum clot strength, primarily reflecting platelet function and fibrinogen contribution 2, 3
• LY30: Percentage of clot lysis 30 minutes after MA, indicating fibrinolytic activity 1, 4

These parameters provide a global hemostatic profile but do not isolate individual coagulation factors 1, 5.

Critical Limitations in Detecting Specific Deficiencies

Cannot Detect Primary Hemostasis Disorders

TEG cannot assess the contribution of endothelium to coagulation, making it unable to detect von Willebrand disease or any conditions affecting endothelial adherence. 1, 2 Because TEG uses reagents that activate coagulation and bypass primary hemostasis, it is insensitive to antiplatelet agents and cannot reliably detect platelet dysfunction 1, 2.

Cannot Quantify Individual Clotting Factors

While a prolonged R time suggests coagulation factor deficiency or anticoagulant effect 2, TEG cannot distinguish which specific factor is deficient 1. For example:

• A prolonged R time could indicate deficiencies in factors II, V, VII, VIII, IX, X, XI, or XII, but TEG cannot differentiate between them 2
• Traditional laboratory measures (PT, aPTT, specific factor assays) remain necessary to identify the exact factor deficiency 1

Limited Sensitivity for Fibrinolysis

TEG shows limited sensitivity in detecting hypofibrinolysis, particularly in pregnancy where fibrinolysis may occur mainly in the placenta rather than systemically 1. The normal reference range for ROTEM CLI30 (94%-100%) makes it impossible to distinguish between normal lysis and hyperfibrinolysis in pregnancy 1.

When TEG Results Are Misleading

Anemia Creates False Hypercoagulability

Anemia can paradoxically show hypercoagulable TEG results (including elevated MA) due to decreased blood viscosity, potentially masking true coagulopathy. 2, 3 This is a common pitfall that can lead to inappropriate withholding of blood products.

Temperature Effects Not Captured

TEG is performed at 37°C and cannot assess the effects of hypothermia on coagulation 2, which is particularly problematic in trauma or massive transfusion scenarios where hypothermia significantly impairs coagulation.

High Variability Between Devices

TEG shows high coefficients of variance (7.1-39.9% for TEG parameters) 2, and results are not interchangeable between TEG and ROTEM devices 2, 3. Device-specific reference ranges must be used 2.

Appropriate Clinical Use of TEG

What TEG Can Guide

TEG is most useful for:

• Detecting global hypercoagulability in pregnancy, showing progressive increases that correlate with gestational age 1
• Guiding transfusion therapy in massive hemorrhage, particularly in cardiac surgery and trauma 5, 6
• Identifying hyperfibrinolysis when LY30 >7.5%, which predicts need for massive transfusion and mortality 1, 4
• Monitoring anticoagulation effects of heparin and direct oral anticoagulants, though sensitivity varies by agent 2

What Requires Additional Testing

When TEG shows abnormalities, specific factor assays, PT/INR, aPTT, fibrinogen levels, platelet count, and platelet function testing remain essential to identify the exact hemostatic defect 1. In liver disease, viscoelastic tests provide more valuable information than standard coagulation tests alone, but interpretation requires careful consideration of the clinical context and supplementation with traditional assays 1.

Practical Algorithm for TEG Interpretation

When faced with abnormal TEG results:

1. Prolonged R time: Check PT/INR, aPTT, specific factor assays, and assess for anticoagulant use 2
2. Decreased MA: Obtain platelet count, fibrinogen level, and consider platelet function testing (not TEG-based) 1, 2
3. Elevated LY30 (>7.5%): Activate massive transfusion protocol and administer tranexamic acid 4
4. Elevated MA: Assess clinical thrombotic risk and consider therapeutic anticoagulation if appropriate 3

TEG provides rapid global hemostatic assessment but must be supplemented with specific laboratory tests to identify individual factor deficiencies and guide targeted therapy. 1, 5